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GW24-e2211 Protective effects of aliskiren on ischaemia-reperfusion-induced renal injury in rats
  1. Liu Yukai1,2,
  2. Zhen Wang1,2,
  3. Yu Han1,2,
  4. Weiwei Guan1,2,
  5. Xun Kou1,2,
  6. Fu Jinjuan1,2,
  7. Di Yang1,2,
  8. Ren Hongmei1,2,
  9. Lin Zhou1,2,
  10. Zeng Chunyu1,2
  1. 1Department of Cardiology, Daping Hospital, The Third Military Medical University
  2. 2Chongqing Institute of Cardiology, Chongqing, PR China


Objectives The protective effect of aliskiren on ischaemia-reperfusion (I/R) injury in the heart and brain has been reported. Whether or not the protective effect exists in renal I/R injury is not known. Therefore, we investigated this effect in kidney in this study.

Methods Sprague-Dawley rats were randomly divided into four groups: sham group; sham control with aliskiren pretreatment; I/R group; I/R with aliskiren pretreatment. Renal ischaemia was induced by occluding the left renal pedicle, and maintained ischaemia for 45 min, the reperfusion lasted for 24 hrs. Aliskiren was administrated 15 min before ischaemia. Blood samples and the kidneys were collected to check for renal function, angiotensin II (Ang II), apoptosis and oxidative stress levels.

Results Compared with the sham rats, serum creatinine (SCR) and blood urea nitrogen (BUN) were significantly increased in I/R rats, accompanied by histopathological damage ofthe kidney, including tubular cell swelling, desquamation, and cast formation. There were more apoptotic cells and leukocyte infiltration in I/R rats than in the sham rats. Pretreatment with aliskiren ameliorated I/R induced renalinjury, i.e. reduced SCR and BUN levels, ameliorated renal histopahological changes, and decreased the apoptosis of cells and leukocyte infiltration in kidney. I/R injury also decreased superoxide dismutase (SOD) and glutathione (GSH-reduced form) levels, which were blocked with the aliskiren pretreatment.

Conclusions Aliskiren pretreatment exerts a protective effect on ischaemia/reperfusion injury in the kidney, via amelioration of oxidative stress, and reduction in leukocyte infiltration and cellular apoptosis.

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